Piezoelectric materials are used in many applications for actuation, sensing, and electric energy harvesting. Piezoelectricity is the ability of crystals to generate a voltage in response to applied mechanical stress. As such, a mechanical stress applied on a piezoelectric material creates an electric charge. Piezoceramics will give off an electric pulse even when the applied pressure is as small as sound pressure. This phenomenon is called the direct piezoelectric effect and is used in sensor applications such as microphones, undersea sound detecting devices, pressure transducers, and electric energy harvesting to power other electronic devices. Piezoelectric materials can also function quite opposite in the converse piezoelectric effect, in which an electric field applied to a piezoelectric material changes the shape of the material as a result of the applied electric energy. In contrast to the direct piezoelectric effect, the converse piezoelectric effect only causes an elongation/contraction of the dipoles in the material causing the entire material to elongate/contract, and does not produce electrical charges. The converse piezoelectric effect makes possible piezoelectric actuators for precision positioning with high accuracy.
Early attempts to suppress organic pain and other neurophysical effects utilizing electrical stimulation occurred as early as about 2,000 years ago when it was discovered that gout apparently could be successfully treated by placing the diseased extremities in a tub of water filled with electric eels. Later, headaches were treated using a similar approach. A detailed, scientific investigation was finally conducted by Professor Galvani of the University of Bologna, which investigation is credited with ultimately leading to the development in the 1800's of electrical equipment for suppression of organic pain.
In 1967, a Dr. Sweet at Massachusetts General Hospital developed the first Transcutaneous electrical nerve stimulation—T.E.N.S. unit. The effectiveness of T.E.N.S. therapy is based on its incorporating two major pain control theories. Under the so-called Gate Control Theory, pain can be inhibited and suppressed by “closing the gate” on pain signals, as such signals arrive at Central Nervous System centers.
This theory postulates that by providing electrical stimulation of a sufficiently high amplitude, the electrical signals race up large myelinated fibers faster than the pain signals travel up smaller myelinated or unmyelinated fibers. The neutral impulses transmitting pain information to the brain thus become interrupted, and since the brain fails to receive the pain signals, no pain is perceived. The other theory incorporated in T.E.N.S. units is the Endorphin Theory, also known as the Endogenous Opiate Theory. This theory postulates that the sustained input of T.E.N.S. signals triggers the release of naturally occurring pain making endorphins and enkephalins (morphine-like substances). These natural substances seemingly block pain signals by a mechanism similar to conventional drug therapy, and inhibit pain information from reaching the brain.
T.E.N.S. therapy is based on a non-invasive, non-narcotic concept of pain management, which is non-addictive, is not subject to abuse, and does not interact with drugs.
T.E.N.S. therapy has already proven to be an effective modality in treating the organic pain problems associated with the following conditions: chronic lumbar and cervical strains or sprains, degenerative disc disease, degenerative arthritic disease, neuropathies, neuralgias, post-lumbar laminectomy syndrome, post-thoracotomy syndrome, bursitis, post phlebitis syndrome, phantom limb syndrome, and tension and migraine headaches.
There are many causes of painful sensory neuropathy. In one subtype referred to as “small-fiber painful sensory neuropathy”, only the A delta (small myelinated) and nociceptive C (unmyelinated) nerve fibers are affected. Studies indicate that this condition represent the most common type of painful sensory neuropathy in patients older than 50 years of age. It is vastly under recognized, and in most cases, no cause can be found. In another group of neuropathies associated with pain, the discomfort has caused in part by damage to small nerve fibers, but large nerve fibers (A beta and A gamma nerve fibers) that are responsible for proprioception, vibratory sensation, muscle-stretch reflexes, and muscle strength are also affected. The distinction between the two subtype painful sensory neuropathies is not trivial, since the underlying cause is most likely to be unidentifiable when both large and small fibers are affected. Irrespective of the subtype of neuropathy, the pain generated by damage to small nerve fibers is debilitating and responds poorly to treatment. Finding and treating the cause is the best long-term strategy, but it is not routinely possible, and even when it is possible, treatment may not be able to relieve pain for many months or longer.
Typical symptoms of neuropathic pain related to small fibers including burning (the sensation that the feet are on fire), sharp pain (described as a knife like jabbing, or pins and needles), shooting pain and aching in the toes and feet (reflecting damage to the longest axons). Pain emanating from the peripheral nerves indicated by the description of the feet as tingling, numb, or feeling tight, wooden, or dead. Peripheral nerve pain if often exacerbated at night, but some patients described pressure-induced pain with standing or walking.
Another cause may include plantar fascitis, arthritis, bursitis, tendonitis, polymyalgia rheumatica, and lumbosacral radiculopathies (with or without spinal stenosis).
The pain in the toes, related to entrapment of the posterior tibial nerve in tarsal tunnel (space beneath the flexor retinaculum and behind the medial malleolus) may mimic painful sensory neuropathy.
Pain can occur without provocation (be stimulus-independent as with burning and paraesthesias accompanying small fiber neuropathies) or can be stimulus evolved (for example, hyperalgesia in response to noxious stimuli or allodynia induced by non-noxious stimuli). The cause of nerve damage does not dictate the type of pain, and non-specific therapies that are effective for one should also be applicable to others.
Summary of Clinical Trials:
Antidepressant aid drugs, 1. Tricyclic antidepressants. i. Amitriptyline. ii. Nortriptyline. iii. Desipramine.
2. Selective Serotonin Reuptake Inhibitors, SSRI.
i. Paroxetine. ii. Citalopram.
Other antidepressants,
ii. Venlafaxine. ii. Bupropion.
Anticonvulsants: 1. Carbamazepine. 2. Phenytoin. 3. Gabapentin.
4. Oxcarbazepine. 5. Lamotrigine. 6. Clonazepam. 7. Topiramate. 8. Pregabalin.
Antiarrhythmic drugs: mexiletine.
Non-narcotic analgesics: Tramadol.
Narcotic analgesics, 1. Oxycodone. 2. Morphine.
Topical anesthetics: 1.5% Lidocaine patch, 2. Capsaicin, 3. NMDA (N-methyl-D-aspartate Glutamate antagonists) Dextromethorphan.
At best, current therapies for painful sensory neuropathy result in 30 to 50% reduction in pain and such a reduction rarely meets patients' expectation.
It remains uncertain whether adequate pain relief can be achieved with a multidrug strategy particularly with the use of pharmacological agents targeted at more than one side in a pain pathway.
At the present time, there are no guidelines available from professional organizations for a treatment of painful sensory neuropathy. (1)
Diabetic neuropathy is a common complication of diabetes. Usually progresses, gradually involves small and large sensory fibers. Symptoms such as loss of ability to sense pain, loss of temperature sensation, and developing neuropathic pain “glove and stocking” distribution, beginning in the lower limbs, first affecting the toes and then progressing upward.
Symptoms of neuropathic pain are commonly reported in patients with the diabetic neuropathy. In one study, 7-13% of the patients had pain and paresthesia when they were diagnosed as having type II diabetes mellitus. The prevalence of pain and paresthesia were 20% and 33% 10 years after diagnosis. (2)
Diabetes was the sixth leading cause of death in the US in 2002. Between 1990 and 2000, number of people in the US diagnosed with diabetes increased by 49%. An estimated 18.2 million Americans now suffered with the disease, with 13 million diagnosed and 5.2 million undiagnosed. If the diabetes prevalence rate were to remain at current levels, the census bureau estimates the number of people diagnosed with diabetes would increase to nearly 14.5 million by 2010 and 17.4 million by 2020.
Diabetic neuropathy is one of the most common, long term complication of diabetes mellitus. Diabetic neuropathy has the highest morbidity and mortality rate and it is associated with a substantial reduction in quality of life. Approximately 20% of patients have neuropathy at the time of diabetes diagnosis, and the number increases to as much as 50% of patients who have had diabetes for 15 or more years.
The patients diagnosed with diabetes and diabetic neuropathy had significant differences in total medical costs. The patient with diabetic neuropathy cohorts had significantly higher mean total medical costs than diabetes mellitus patient ($24,765 versus $4819). This increase in cost associated with diagnosis of neuropathy included all cost component: Inpatient ($7282 versus $1005), outpatient ($14,137 versus $2548), emergency room ($889 versus $178), and a pharmaceutical ($6526 versus $1098) costs. The patient diagnosed with diabetes had a mean total diabetes related medical cost of $1297; however, with the addition of neuropathy complication the mean total diabetes related cost with significant increase to $5125 for the diabetic neuropathy patient. (3)
Peripheral neuropathy is one of the most common complications of both type 1 and type 2 diabetes. In a population-based study, 22% of the diabetic cohort had peripheral neuropathy that was moderate to severe. Long standing peripheral neuropathic pain associated with peripheral neuropathy occurs in one of six diabetic subjects. When symptoms are present, they may be negative or positive. Negative symptoms include loss of sensation and loss of strength, while positive symptoms include pricking or pain. One of the most distressing symptoms that people can suffer from is neuropathic pain and paresthesia. Chronic painful peripheral neuropathy is common and often severe, but frequently unreported and inadequately treated. (4)
Diabetes mellitus is one of the most common chronic medical condition affecting over 100 million people worldwide of whom up to 60% may develop diabetic polyneuropathy.
The pain transmission via the axons, which is manifested as either a small myelinated (A delta) or thinner unmyelinated (C) fibers each performing specific tasks. Somatic pain arises from the skin, muscles, or joints and can be classed as either superficial or deep. Superficial pain is often sharp or pricking sensation and is transmitted along the fine lightly myelinated A delta fibers. Alternatively, deep somatic pain, often a burning, itching, or aching type of pain with longer duration arising from the deep layers of soft tissue or joint. In normal condition, this form of pain almost always indicates tissue damage and is conducting along the slower unmyelinated C-fibers. (5)
The main advantage of TENS system is its portable nature as a topical application of low-frequency currents making it safe. TENS machines are clearly contraindicated in patients with pacemakers. (5)
A trial conducted by Meyler (6) evaluated the use of TENS in 200 patients with a variety of pain syndromes. The results demonstrated that 53% with peripheral nerve damage reported pain reduction.
Neuropathic pain is characterized by abnormal stimulus-evoked pain, which is usually described as hypersensitivity. It can result from injuries to the peripheral sensory nerve. Hypersensitivity is defined as a condition of extreme discomfort or irritability in response to normally non-noxious tactile stimulation. Neuropathic pain (hypersensitivity) can be subdivided into hyperalgesia and allodynia. The International Association for the Study of Pain (IASP) define hyperalgesia as a greater than normal pain response to painful stimuli, and the term allodynia refers to pain produced by a normally non-painful stimulus.(7)
In the clinical settings, Transcutaneous Electrical Nerve Stimulation (TENS) is one of the commonest treatments for hypersensitivity. (7)
Between 80-85% of patients experienced beneficial effect of electrotherapy for neuropathic pain. Combination of therapy with amitriptyline and electrotherapy appears to be superior to either drug or electrotherapy alone.
Because symptoms would recur when electrotherapy discontinued, it appears a maintenance treatment protocol should be developed for each patient. TENS device generated a biphasic, exponentially decaying waveforms with pulse. (8)
There is some suggestion that the TENS may have an effect for central post-stroke pain, visuo-spatial neglect, and neglect-related postural instability. Transcutaneous electric nerve stimulation may have a possible use as a sensory stimulus to rehabilitate sensory function or as a sensory prosthesis to boost sensory perception and subsequent functional activity. (9)    1. Painful sensory neuropathy Jerry R. Mendell, M.D and Varise Sahenk, M.D, PhD. New England Journal of Medicine 348; 13-Mar. 27, 2003.    2. Effects of Treatments for Symptomatic and Painful Diabetic Neuropathy:    Systemic review by Man-Chun Wong, Joanne W, Y. Chung, and Thomas S. Wong B M J 2007; 335; 87 originally published on Jun. 11, 2007.    3. Resource use among patients with diabetes, diabetic neuropathy, and diabetes with depression by Trong K. Le, Stephe N. Able, and Maureen J. Lage. Cost Effectiveness and Resource Allocation 2006, 4:18 published on Feb. 23, 2006.    4. The Prevalence, Severity, and Impact of Painful Diabetic Peripheral Neuropathy in Type 2 Diabetes by Mark Davies, MSC, Sinead Brophy, Ph.D., Rhys William Ph.D., and Ann Taylor, MSC from diabetes care, Volume 29, #7, July 2006.    5. The Pathogenesis and Management of Painful Diabetic Neuropathy: A Review by M. C. Spruce, J. Potter, and D. V. Coppini. Diabetic Medicine, 20, 88-98 in 2003.    6. Meyler W J, De Jongste M J, and Rolf C clinical evaluation of pain and treatment with electrostimulation: A study of TENS in patient with different pain syndrome. Clinical Journal of Pain in 1994: 10:22-27,    7. Transcutaneous Electrical Nerve Stimulation for Neuropathic pain by G. L. Y. Cheing and M. L. M. Luk Journal of Hand Surgery (British and European volume, 2005) 30B, column 1, column 50-55.    8. Transcutaneous electrostimulation: Emerging Treatment for Diabetic Neuropathy Pain by Michael Alvero, DPM, Dinesh Kumar, M.D., and    Inderjeet S. Julka, M.D. Diabetes Technology and Therapeutics Volume#1, 1999, pages 77 to 81.    9. Use of Transcutaneous Nerve Stimulation to Treat Sensory Loss After Stroke by Sarah Tyson from Physiotherapy Research International, 8 (1) 53-57, 2003.
As discussed above, it has been proven that electrical energy can have therapeutic effect on human or animal tissue, muscles, and other physiological areas. There are a variety of methods and devices on the market that use this technique. For example, what is known as a TENS unit or device converts electrical energy from an external alternating current (AC) source or a battery into an electrical field that is applied to an injured or targeted portion of the body.
One problem with known devices and systems is they require an external or battery electrical power source. This usually means either limited mobility during treatment or added weight and bulk, which can be counterproductive or cumbersome for the user. Furthermore, most devices, including TENS devices, require electrodes to be adhesively placed on a targeted location of the body. Most times, the electrodes then must be hard-wired to a control unit. This is cumbersome to install and wear. It requires immobilization of the user to place the electrodes or remove them.
Many existing devices are also relatively expensive, and require close monitoring or even operation by health care professionals.
There is a real need in this area for improvement. For example, there is a real need for technology that utilizes the benefits of electrical fields for therapeutic purposes, but with less constrictions on mobility of the user during treatment. There is also a need for a more efficient and economical method for administering such therapy.